A variety of host mechanisms appear to control or modify the colonization and growth or oral microorganisms. However, little is known about the interactions of these immune system components in controlling the bacteria associated with the development of periodontal disease. Current evidence suggests that gingival health as well as specific forms of the disease are associated with specific microflora. Overall, progression of periodontitis appears associated with a shift to more anaerobic, Gram negative bacteria. A particular form, localized juvenile periodontitis (LJP) has exhibited a strong experimental association with strains of Actinobacillus actinomycetemcomitans (Aa), a Gram-negative, facultative anaerobe. LJP occurs predominantly in peripubertal females without significant clinical evidence of inflammation. Defective chemotaxis and defective bacterial killing by PMN's of LJP patients have been demonstrated, as well as elevated lgG and lgA titers to specific Aa strains. Using LJP as a model for host-parasite interaction, it is proposed to assess the separate and collective effects of various host mechanisms and environmental parameters on the growth kinetics and viability of selected strains of Aa and Bacteroides gingivalis, an obligate Gram-negative anaerobe associated with more chronic forms of periodontal disease. Characterization of the effects of host anti-microbial mechanisms on these organisms under various aerobic and anaerobic conditions may have important implications by reflecting the in vivo microenvironments available to these suspected periodontal pathogens. The effects of lactoferrin, lactoperoxidase, myeloperoxidase and lysozyme will be assessed under different 02 concentrations. The extent of neutrophil dysfunction in the LJP patients will be evaluated by extraction, purification, quantitative immunoelectrophoresis and immunoblotting of the enzymes found in their granules including myeloperoxidase, lactoferrin and lysozyme. In addition, recent reports suggest a possible synergistic effector function for slgA and PMN's. PMN's from the blood and gingival crevice will be collected and examined by cytofluorography for lgA and IgG receptors. LJP serum and secretory immunoglobulins will be examined for opsonic activity and synergistic killing of test strains. These investigations will help define the mechanisms by which the immune system exerts selective control over the complex oral microflora. Specific enhancement or down-regulation of this selection process may provide new therapeutic techniques for disease control.